PE23.1-21 | Gastrointestinal and Hepatobiliary System — Practice Quiz

Bilious vomiting in a neonate/young infant must be treated as a surgical emergency until proven otherwise. Malrotation with volvulus causes bilious vomiting, abdominal distension, and can rapidly lead to intestinal gangrene.

Any bilious (green) vomiting in an infant is a surgical emergency until proven otherwise — act on the assumption of malrotation with volvulus; do not delay imaging or surgical consultation.

GERD causes non-bilious regurgitation; pyloric stenosis causes non-bilious projectile vomiting; overfeeding causes non-bilious spitting. Bilious vomiting = surgical emergency (malrotation/volvulus, intestinal atresia, Hirschsprung's).

USG criteria for HPS: pyloric muscle thickness >3–4 mm AND pyloric channel length >14–16 mm. These are the established sonographic thresholds for diagnosis.

Hypertrophic pyloric stenosis presents at 2–8 weeks with non-bilious projectile vomiting and a hungry baby; USG diagnoses with muscle thickness >3–4 mm and channel length >14–16 mm. Metabolic consequence: hypochloraemic, hypokalaemic metabolic alkalosis.

Muscle thickness of 2 mm is within normal range. Antral wall thickness and pyloric opening diameter are not the standard sonographic criteria for HPS diagnosis.

A narrow rectosigmoid segment with a proximal funnel-shaped transition zone on barium enema is the hallmark of Hirschsprung disease (aganglionic megacolon). The aganglionic segment fails to relax, causing functional obstruction.

Hirschsprung disease is diagnosed by barium enema (transition zone) and confirmed by rectal suction biopsy showing absent ganglion cells. Key differentiator from functional constipation: onset at birth and failure to pass meconium within 48 hours.

Functional constipation has a normal barium enema, no transition zone, and typically starts after birth. Hypothyroidism causes constipation but not a structural transition zone. Anal fissure causes pain-related withholding, not a narrow rectosigmoid segment.

Sunken eyes, reduced skin turgor, irritability, reduced urine output = some dehydration (Plan B). WHO Plan B: give 75 mL/kg of reduced-osmolarity ORS (osmolarity 245 mOsm/L) over 4 hours, with reassessment. Plan B is administered at a health facility.

WHO IMNCI classifies dehydration as no, some, or severe. 'Some dehydration' = Plan B (75 mL/kg ORS over 4 hours). Use reduced-osmolarity ORS (osmolarity 245 mOsm/L) — not standard 311. Reassess after 4 hours.

Plan A is for no signs of dehydration. Plan C (rapid IV fluids) is for severe dehydration (lethargic, unable to drink, no urine). IV antibiotics are not indicated for viral gastroenteritis.

For children ≥6 months, WHO recommends zinc 20 mg/day for 14 days as part of diarrhoea management. For children <6 months, the dose is 10 mg/day for 14 days. The duration is 14 days regardless of the age group.

WHO zinc for diarrhoea: ≥6 months = 20 mg/day × 14 days; <6 months = 10 mg/day × 14 days. Zinc shortens diarrhoea duration and reduces recurrence — it is a fixed 14-day course regardless of clinical resolution.

The duration is always 14 days. The dose is age-dependent: <6 months = 10 mg/day; ≥6 months = 20 mg/day. This child is 2 years old, so 20 mg/day for 14 days is correct.

Shigella dysentery is treated with antibiotics (reduces duration and complications). Azithromycin (10–12 mg/kg/day for 3 days) is the current first-line agent due to widespread resistance to co-trimoxazole and ampicillin. Nalidixic acid resistance is also common.

Shigella dysentery: treat with azithromycin (first-line due to co-trimoxazole resistance). EHEC dysentery: antibiotics are CONTRAINDICATED (HUS risk). Amoebic dysentery: metronidazole 10 mg/kg/dose TDS × 10 days. Know the pathogen before choosing the antibiotic.

Metronidazole is used for amoebic dysentery, not bacillary (Shigella). Co-trimoxazole was previously first-line but widespread resistance now limits its use. EHEC (E. coli O157:H7) dysentery is the case where antibiotics are contraindicated due to HUS risk — NOT Shigella.

Elevated anti-tTG IgA (with normal total IgA) plus villous atrophy on duodenal biopsy = coeliac disease. The cornerstone of treatment is a strict, lifelong gluten-free diet (avoid wheat, barley, rye). Anti-tTG IgA can be falsely low in IgA deficiency — checking total IgA is essential.

Coeliac disease: screen with anti-tTG IgA + total IgA (to exclude selective IgA deficiency); confirm with duodenal biopsy (Marsh ≥2 villous atrophy). Treatment: strict, lifelong gluten-free diet. CF is diagnosed by sweat chloride >60 mEq/L on two occasions.

CF presents with steatorrhoea, recurrent chest infections, and sweat chloride >60 mEq/L. Lactose intolerance causes bloating and watery diarrhoea without villous atrophy. Tropical sprue responds to folate + tetracycline — but the biopsy pattern and serology here confirm coeliac disease.

HAV hepatitis is self-limiting — treatment is supportive (rest, hydration, nutritious diet, avoid hepatotoxic drugs and alcohol). Anti-HAV IgM confirms acute infection. Infectious period is 2 weeks before jaundice to 1 week after — not 6 months. Entecavir is for hepatitis B (chronic). Steroids are NOT used.

Hepatitis A: faeco-oral transmission, anti-HAV IgM = acute infection, supportive treatment, excellent prognosis, no chronicity. Hepatitis E also causes acute hepatitis with faeco-oral transmission (dangerous in pregnancy). HBV and HCV can cause chronic disease.

Entecavir is a nucleoside analogue for chronic HBV. HAV does not cause chronic liver disease — no antiviral is needed. Steroids are not indicated in acute viral hepatitis and may be harmful. Isolation is needed for 1 week after jaundice onset, not 6 months.

Acute liver failure (FHF) in a previously healthy child: jaundice + encephalopathy + coagulopathy (INR >1.5) within 8 weeks of illness onset, no prior liver disease. Coagulopathy (INR/PT) and grade of encephalopathy are the key prognostic indicators and criteria for urgent liver transplant listing.

Fulminant hepatic failure (FHF): jaundice + coagulopathy + encephalopathy within 8 weeks, no prior liver disease. Top causes in children: viral hepatitis (HAV, HEV), Wilson disease, drug-induced. Prognostic indicators: PT/INR and encephalopathy grade. Manage in a liver transplant centre.

Chronic liver disease with decompensation would have prior liver disease, cirrhotic features. Biliary atresia presents with neonatal cholestasis. Wilson disease can cause FHF but ceruloplasmin is not the prognostic indicator (PT/INR and encephalopathy grade are).

EHPVO is the commonest cause of portal hypertension in Indian children. History of umbilical vein catheterisation (or neonatal sepsis) plus normal liver function and splenomegaly with variceal bleeding = EHPVO. Normal LFTs distinguish it from intrahepatic (cirrhotic) portal hypertension.

EHPVO is the most common cause of portal hypertension in Indian children. Normal LFTs + history of neonatal umbilical vein catheterisation + cavernous transformation on portal vein Doppler = diagnostic. Management: endoscopic variceal ligation + beta-blockers; TIPS or meso-Rex bypass for selected patients.

Chronic hepatitis B would have abnormal LFTs and liver architecture changes. Hepatocellular carcinoma would have a hepatic mass. Budd-Chiari involves hepatic venous outflow obstruction (hepatomegaly, ascites, abdominal pain), typically with abnormal LFTs.